We have observed changes in the ion and water content of vascular walls occurring in normotensive vascular beds of chronic hypertensive animals (coarctation, or 1- or 2-kidney renal). Therefore, elevated intravascular pressures are not necessary for the development of such vascular changes and other causative mechanisms must be sought. We propose to investigate the role of other variables, including age, cellular hypertrophy or hyperplasia, renin and other "renal factors". Because we have evidence that the activity of the cellular ouabain-sensitive sodium-potassium pump is decreased in vascular tissue of animals with chronic renal hypertension, we also propose to investigate the relationship between the activity of this pump and abnormalities of vascular wall composition in several forms of hypertension. Finally, if indicated by our results, we propose to attempt to identify plasma factors responsible for reduction in pump activity in hypertension.